Expression of ALS1, HWP1 and SAP4 genes in Candida albicans strains isolated from women with vaginitis

T Nas1, A Kalkanci, I Fidan

  • 1Department of Gynecology and Obstetrics, Gazi University, Ankara, Turkey.

Folia Microbiologica
|October 8, 2008
PubMed

Insights

This study investigated gene expression in Candida strains from vaginal swabs. Key adhesion genes (ALS1, HWP1) and SAP4 showed varied expression in vulvovaginal candidiasis, independent of estrogen levels.

Area of Science:

  • Mycology
  • Molecular Biology
  • Gynecology

Background:

  • Vulvovaginal candidiasis (VVC) is a common infection.
  • Candida albicans virulence factors, including adhesion genes, play a role in VVC pathogenesis.
  • Estrogen levels can influence VVC susceptibility and potentially gene expression.

Purpose of the Study:

  • To investigate the in vivo gene expression of SAP4, ALS1, and HWP1 in Candida strains isolated from women with VVC.
  • To determine if gene expression correlates with patient demographics (pregnant, postmenopausal, reproductive age) and estrogen levels.

Main Methods:

  • Total mRNA was extracted from Candida strains isolated from vaginal swabs.
  • Reverse-transcriptase polymerase chain reaction (RT-PCR) was used to quantify the expression of SAP4, ALS1, and HWP1 genes.
  • Gene expression profiles were analyzed across different patient groups.

Main Results:

  • The expression of ALS1, HWP1, and SAP4 genes was detected in 69%, 62%, and 38% of VVC cases, respectively.
  • Specific expression patterns were observed for ALS1, HWP1, and SAP4 across pregnant, postmenopausal, and reproductive age groups.
  • No correlation was found between the expression of these adhesion genes and the estrogen levels of the patients.

Conclusions:

  • The adhesion genes ALS1 and HWP1, along with SAP4, are expressed in vivo during VVC.
  • Gene expression profiles vary among different patient groups but do not appear to be influenced by estrogen levels.
  • These findings contribute to understanding Candida virulence mechanisms in VVC.